The transcription factor Tcf21 is necessary for adoption of cell fates by Foxd1 + stromal progenitors during kidney development
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This study identifies Tcf21 as a key regulator of kidney stromal fate. Loss of Tcf21 disrupts the emergence of key stromal cell types and leads to the expansion of a dysregulated, Emcn-expressing stromal population. Integrating single-cell transcriptomics, chromatin accessibility, and histology, we show that this misdifferentiation contributes to fibrosis in adulthood. These findings suggest that TCF21-dependent stromal differentiation restrains maladaptive remodeling and links developmental fate decisions to later fibrotic disease.
